A synaptic vesicle will fuse with the membrane of the presynaptic cell and will release its content into the synaptic cleft after action potential has been reached. The relationship between a synaptic vesicle and a neurotransmitter is that the synaptic vesicle will contain neurotransmitter which are macromolecules that neurons use to communicate with each other. For worms, the synaptic vesicles release acetylcholine which will go into the synaptic cleft cause by electrical impulses that go down the axon (http://www.worm)
The 5 worms that my group observed in plate A were the wild type strain and all 5 worms were constantly moving ventral to dorsal for the entire minute. The worms moved like a snake, from head to tail. The 5 worms that my …show more content…
One worm was stationary the whole minute observed, another moved its’ head for 20 seconds, then moved its’ body for 10 seconds and then was stationary but occasionally moved its’ head for 30 seconds, another coiled for 10 seconds, uncoiled for 30 seconds, moved only its’ head for 10 seconds and then it’s body started to move away for another 10 seconds. Another bumped into another worm for 30 seconds, coiled for 20 seconds and wiggled for 10 seconds, the last one did not move the whole time. Overall, the worms in plate C did not move much, if hardly at all. The movement of the wild type worms differed from the movement of the two mutant strains of worms as the wild type moved faster and could use most of their body unlike the defect ones which moved lethargically and struggled to move at all.
Type B worms were the ones that had a strain defect in synaptic vesicle transport. This was because this defect had a mutation in gene coding for motor protein, kinesin. That would mean that the action potential would struggle to travel to the axon toward the terminal to trigger synaptic vesicles. However, by chance, the synaptic vesicle could still be triggered and cause muscle contraction in the worm. The effect of this mutation on worm movement would be that the worms still moved, but slower and a lot less than the wild type
The 5 worms that my group observed in plate A were the wild type strain and all 5 worms were constantly moving ventral to dorsal for the entire minute. The worms moved like a snake, from head to tail. The 5 worms that my …show more content…
One worm was stationary the whole minute observed, another moved its’ head for 20 seconds, then moved its’ body for 10 seconds and then was stationary but occasionally moved its’ head for 30 seconds, another coiled for 10 seconds, uncoiled for 30 seconds, moved only its’ head for 10 seconds and then it’s body started to move away for another 10 seconds. Another bumped into another worm for 30 seconds, coiled for 20 seconds and wiggled for 10 seconds, the last one did not move the whole time. Overall, the worms in plate C did not move much, if hardly at all. The movement of the wild type worms differed from the movement of the two mutant strains of worms as the wild type moved faster and could use most of their body unlike the defect ones which moved lethargically and struggled to move at all.
Type B worms were the ones that had a strain defect in synaptic vesicle transport. This was because this defect had a mutation in gene coding for motor protein, kinesin. That would mean that the action potential would struggle to travel to the axon toward the terminal to trigger synaptic vesicles. However, by chance, the synaptic vesicle could still be triggered and cause muscle contraction in the worm. The effect of this mutation on worm movement would be that the worms still moved, but slower and a lot less than the wild type